Accepted Manuscript

Title: Harm expectancy violation during exposure therapy for

posttraumatic stress disorder

Authors: Rianne A. de Kleine, Lotte Hendriks, Eni S. Becker,

Theo G. Broekman, Agnes van Minnen

PII: S0887-6185(16)30104-9
DOI: http://dx.doi.org/doi:10.1016/j.janxdis.2017.03.008
Reference: ANXDIS 1931

To appear in: Journal of Anxiety Disorders

Received date: 20-6-2016

Revised date: 10-3-2017
Accepted date: 29-3-2017

Please cite this article as: de Kleine, Rianne A., Hendriks, Lotte., Becker, Eni S.,
Broekman, Theo G., & van Minnen, Agnes., Harm expectancy violation during
exposure therapy for posttraumatic stress disorder.Journal of Anxiety Disorders
http://dx.doi.org/10.1016/j.janxdis.2017.03.008

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Harm expectancy violation during exposure therapy for posttraumatic stress disorder.

Rianne A. de Kleine, PhD1,2; Lotte Hendriks, MSc 2,3; Eni S. Becker, PhD 3; Theo G. Broekman, Msc4;

and Agnes van Minnen, PhD 2,3

1
Institute of Psychology, Leiden University, The Netherlands; 2 Center for Anxiety Disorders

Overwaal, Institution for Integrated Mental Health Care Pro Persona, Nijmegen, the Netherlands; 3

Radboud University, Behavioural Science Institute, NijCare, Nijmegen the Netherlands; 4 Bureau

Beta, Nijmegen, The Netherlands

Corresponding author: Rianne de Kleine, Institute of Psychology, Leiden University, Wassenaarseweg

52, P.O. Box 9555, 2300 RB Leiden, the Netherlands; Tel. +31 715277672;

r.a.de.kleine@fsw.leidenuniv.nl

Highlights:

 Prior to exposure therapy, PTSD patients had relatively high harm expectancies and

almost all patients feared their own reactions to imaginal exposure.

 Exposure therapy promoted harm expectancy violation.

 Harm expectancy violation was not related to treatment outcome.

 Fear habituation, both within and between session, was positively related to treatment

outcome.

Abstract

Exposure therapy has proven efficacy in the treatment of posttraumatic stress disorder (PTSD).

Emotional processing theory proposes that fear habituation is a central mechanism in symptom

reduction, but the empirical evidence supporting this is mixed. Recently it has been proposed that

violation of harm expectancies is a crucial mechanism of action in exposure therapy. But to date,

changes in harm expectancies have not been examined during exposure therapy in PTSD. The goal of

1
the current study was to examine harm expectancy violation as mechanism of change in exposure

therapy for posttraumatic stress disorder (PTSD). Patients (N=50, 44 female) with a primary

diagnosis of chronic PTSD received intensive exposure therapy. Harm expectancies, harm experiences

and subjective units of distress (SUDs) were assessed at each imaginal exposure session, and PTSD

symptoms were assessed pre- and posttreatment with the Clinician Administered PTSD Scale (CAPS).

Results showed that harm expectancies were violated within and strongly declined in-between

exposure therapy sessions. However, expectancy violation was not related to PTSD symptom change.

Fear habituation measures were moderately related to PTSD symptom reductions. In line with theory,

exposure therapy promotes expectancy violation in PTSD patients, but this is not related to exposure

therapy outcome. More work is warranted to investigate mechanisms of change during exposure

therapy in PTSD.

Keywords: expectancy violation; fear habituation; exposure therapy; PTSD; mechanisms of change

2
1. Introduction

Exposure therapy has proven efficacy for the treatment of posttraumatic stress disorder

(PTSD). In emotional processing theory (Foa & Kozak, 1986), it has been argued that fear

habituation1 both within and between sessions, denotes exposure therapy success. However,

studies investigating the predictive value of fear habituation (as indexed by a decrease in

subjective units of distress (SUD) ratings) for treatment outcome have yielded mixed findings

(Bluett, Zoellner, & Feeny, 2014; Rauch, Foa, Furr, & Filip, 2004; Sripada & Rauch, 2015).

Extinction learning is thought to be one of the mechanisms of action in exposure therapy, and

refers to the process in which a conditioned stimulus (CS; i.e., a trauma reminder) is

repeatedly presented in the absence of the unconditioned stimulus (US; i.e., the traumatic

experience) thereby leading to reduction of the conditioned response (CR; i.e., fear). It is now

believed that extinction learning is not so much the deletion of the original CS-US

association, but rather a new learning of a CS – No US relationship (Bouton, 1993), referred

to as inhibitory learning (Craske et al., 2008). According to the theory of inhibitory learning,

extinction occurs after a mismatch between the expectancy of an aversive event and the

absence of its occurrence (Rescorla & Wagner, 1972), i.e. violation of the harm expectancy.

Translated to exposure therapy for PTSD, this means that a PTSD patient learns that

confrontation with traumatic stimuli (CS) will not lead to the expected hazardous outcome

(No US). Hypothetically, as an alternative to the fear habituation model, violation of the idea

that exposure to trauma-related stimuli would be harmful could lead to successful extinction

learning and favourable treatment outcome in the end. Although this expectancy violation

hypothesis has been affirmed by both theory and experimental work (Craske, et al., 2008;

Craske, Treanor, Conway, Zbozinek, & Vervliet, 2014), there are no studies that have tested

1
Note that the process referred to is not actual fear habituation, but rather extinction learning.
However, to align with the terminology of EPT we will refer to this process as fear
habituation throughout this report.
3
harm expectancy violation as mechanism of change in exposure therapy for PTSD. In

experimental fear conditioning paradigms changes in harm (US) expectancies are often used

as an indication of successful extinction learning (Boddez et al., 2013), and there is evidence

to suggest that PTSD patients are characterized by elevated harm expectancies during

experimental extinction learning (Blechert, Michael, Vriends, Margraf, & Wilhelm, 2007).

Moreover, this this expectancy bias was found to predict the onset (Lommen, Engelhard,

Sijbrandij, van den Hout, & Hermans, 2013) and maintenance (Engelhard, de Jong, van den

Hout, & van Overveld, 2009) of PTSD symptoms. However, to the best of our knowledge,

there is no study investigating expectancy violations during exposure therapy for PTSD. As

such, it is still unclear which harm expectancies should be targeted and violated during

exposure therapy for PTSD in order to optimize learning. There is ample evidence that

cognitive changes occur during exposure therapy, even without explicitly addressing

dysfunctional cognitions (Foa et al., 2005; Hagenaars, van Minnen, & de Rooij, 2010;

McLean, Yeh, Rosenfield, & Foa, 2015; Zalta et al., 2014), and that these cognitive changes

precede PTSD symptom decline (McLean, et al., 2015; Zalta, et al., 2014). However, in these

studies general dysfunctional cognitions were studied and not so much expectancy violations.

Investigating changes in the CS-US relationship could provide us with a better understanding

of the mechanisms of change during exposure therapy.

The aims of this study are: 1) to gain more insight into harm expectancies during

exposure therapy for PTSD; 2) to examine whether harm expectancies are violated during

exposure therapy; 3) to examine whether harm expectancy violation is related to exposure

therapy outcome; and 4) to explore the relationship between expectancy violation and fear

habituation during exposure therapy.

2. Materials and methods

2.1 Participants

4
Participants were 50 treatment-seeking patients (44 women, mean age = 37 year) with a primary

diagnosis of DSM-IV defined chronic PTSD (as established by the MINI; (Sheehan et al., 1998)

following interpersonal victimization (see table 1). All were enrolled in an open exposure therapy

trial. Those with acute suicidal risk and inadequate proficiency of the Dutch language were excluded

from participation. Written informed consent was obtained from all participants. Prior to enrolment,

PTSD diagnoses were verified by means of the Clinician Administered PTSD Scale (Blake et al.,

1990), and mean scores indicated severe PTSD symptoms (M= 83.68, SD = 13.83).

2.2 Measures

Clinician Administered PTSD Scale (Blake, et al., 1990). Outcome was assessed with the Dutch

translation of the Clinician-Administered PTSD Scale (CAPS-1; Blake et al., 1995; Hovens, Luinge,

& van Minnen, 2005), a clinician-rated structured interview developed to test for the presence of the

17 DSM-IV-TR criteria for PTSD.

Subjective Units of Distress (SUDs). During each exposure session subjective units of distress

ratings ((SUDs; Wolpe, 1958)) were obtained. Participants rated their levels of distress on a 0-10 point

scale (no anxiety - maximum anxiety). Following previous studies (e.g. Rauch, et al., 2004; Rothbaum

et al., 2014; van Minnen & Hagenaars, 2002), within session habituation was calculated by subtracting

the end of exposure SUD score from the peak SUD score, and between session habituation was

calculated as the difference between SUD peak scores from successive sessions. The mean of these

differences were used as indices of average within- and between session habituation over treatment.

Harm expectancy and Harm experience ratings. To gain more insight into harm expectancies in

PTSD patients, at the start of treatment, participants formulated their harm expectancy regarding

imaginal exposure by completing an open-ended sentence: “Doing imaginal exposure, I fear....”. In

addition, to assess changes in harm expectancy ratings over treatment participants rated their belief in

three commonly expressed harm expectancies regarding (imaginal) exposure (Craske, et al., 2014; Foa

& Kozak, 1986; Foa & Rothbaum, 1998) prior to each exposure session on a 0 (totally disagree) to 10-

point (completely agree) scale. These expectancies were: During imaginal exposure I will get so

5
anxious, that I will: 1) go crazy; 2) lose control; 3) panic. Immediately after each session, participants

rated their harm experience. That is, they rated (on a scale from 0 (not at all) to 10 (completely))

whether they actually experienced their feared outcome, i.e. had the feeling they went crazy, lost

control, or panicked. Internal consistency of both the harm expectancy and experience questionnaire

was deemed satisfactory (α =.94 and α =.90, respectively), hence we used mean scores of both

measures in all analyses. In analogue to the fear habituation measures, we calculated within session

expectancy violation by subtracting harm experience from harm expectancy ratings and between

session expectancy change by subtracting harm expectancy scores from successive sessions. The mean

of these differences were used as indices of average expectancy violation and change over treatment.

2.3 Procedure

Prior to treatment all participants completed a baseline assessment, comprising clinician

administered and self-report instruments. Treatment consisted of brief intensive exposure

therapy (Hendriks, de Kleine, van Rees, Bult, & van Minnen, 2010), which is largely based

on the Prolonged Exposure (PE) protocol (Foa, Hembree, & Rothbaum, 2007). The intensive

phase comprised 12 exposure-based sessions provided on four consecutive treatment days.

Each day’s first session consisted of manualized 60 minute imaginal exposure following the

PE protocol. Patients were instructed to close their eyes and recount the traumatic memories

aloud. Following these imaginal exposure sessions, patients engaged each day in two more

exposure sessions, that included imaginal exposure but also additional exposure-based

treatment components (such as in-vivo exposure). To align with previous studies in this field

(Bluett, et al., 2014; Rauch, et al., 2004; van Minnen & Foa, 2006; van Minnen & Hagenaars,

2002) and limit variance due to different treatment procedures, we only assessed expectancy

violation and fear habituation during the imaginal exposure sessions that followed the PE

protocol. The intensive phase was followed by a maintenance phase, wherein participants

received up to four weekly exposure-based booster sessions. One week after completion of

6
the total treatment program (six weeks), participants (N=48, 2 missing) completed the post-

treatment assessment.

3. Results

Self-reported harm expectancies prior to the first exposure session

At the start of treatment, using the open-ended sentence, almost all participants (96%, N=48) reported

harm expectancies related to their responses to exposure, and only two participants (4%) reported fear

of external threat (i.e. that the offender would re-appear). Examples of the reported harm expectancies

were: “I will go crazy”; “I won’t be able to control my emotions”; “ I will get verbally aggressive”;

and “I will freak out”.

Harm expectancy changes over treatment

Prior to the first exposure session, mean harm expectancy ratings were 6.45 (SD=2.43, see table 2),

and these ratings were not significantly related to pre-treatment PTSD symptom severity as measured

by the CAPS (r =.19, p =.200). As can be seen in table 1, harm expectancy ratings significantly

declined between imaginal exposure sessions on day 1 and 2, t = 5.40, p = <.001, between day 2 and 3,

t = 3.00, p=.004, and between day 3 and 4, t = 2.64, p =.011.

Expectancy violation as a predictor of PTSD symptom reduction following treatment

PTSD symptoms significantly declined over the course of treatment (CAPS scores pre treatment: M =

85.79 (range: 47-116; SD = 15.46); post treatment M = 61.27 (range: 2-109; SD =31.05; Cohen’s d

=1.01). Neither within session expectancy violation (r = .02, p =.875) nor between session expectancy

change (r = -.19, p = .185) was significantly related to CAPS residual gain scores (Steketee &

Chambless, 1992).

Exploring the relationship between expectancy violation and fear habituation

7
Averaged within session expectancy violation and within session fear habituation were not

significantly related (r = .09, p = .547). As to the between session measures, expectancy changes and

fear habituation were significantly related (r = .39 p = .002), suggesting that those with a greater

decline in harm expectancies over treatment sessions also had a greater fear decline over sessions (see

table 3).

Relating the fear habituation measures to CAPS gain scores, both within (r = -.40, p = .005)

and between session habituation (r = -.30. p = .037) were related to CAPS residual gain scores.

Tentatively, expectancy violation and fear habituation measures are especially predictive of treatment

response when they occur in synchrony. To test this hypothesis, we ran a stepwise regression analysis

entering all expectancy violation and fear habituation indices in the first step, and these indices plus

their interaction (i.e. within session expectancy violation × within session habituation; between session

expectancy change × between session habituation) in the second step. The overall model was

marginally significant in the first step (R2=.19, p = .052), with within session habituation being the

only significant predictor (ß = -.34, p =.036). Including the interaction terms did not improve the

overall model (R2 change = .02, p =.644, besides within session habituation all ß’s non significant).

Given that PTSD is a very heterogeneous disorder and expectancy violation might be

specifically related to the more fear-based PTSD symptoms, we additionally explored the relationship

between expectancy violation and changes in different PTSD symptom clusters. Following King and

colleagues (1998), we calculated residual gain scores for the symptom clusters re-experiencing,

avoidance, dysphoria and hyperarousal. These four symptom clusters map nicely onto DSM-5 defined

PTSD. The results of these exploratory symptom cluster analyses were similar to those of the primary

analyses.

4. Discussion

The primary aim of this study was to investigate harm expectancy violation during imaginal

exposure therapy in PTSD. We showed that: (1) patients had harm expectancies regarding

their own reaction to exposure; (2) harm expectancies were violated within sessions and

strongly declined between sessions; (3) neither within session expectancy violation nor

8
between session expectancy change was related to PTSD symptom change; (4) between

session expectancy change and fear habituation were moderately related; and (5) fear

habituation was moderately related to gains in PTSD symptoms.

Prior to treatment, PTSD patients had relatively high harm (US) expectancies regarding

trauma memory recollection, a finding that resembles the previously demonstrated expectancy

bias in PTSD patients (Blechert, et al., 2007; Engelhard, et al., 2009; Lommen, et al., 2013).

The strong decline in harm expectancies indicates that patients successfully learned that

confrontation with their traumatic memories did not lead to the expected harm (i.e. acquisition

of a CS-no US association). This finding is in line with previous work showing that exposure

therapy promotes cognitive change (Hagenaars, et al., 2010; McLean, et al., 2015; Nacasch et

al., 2015; Zalta, et al., 2014), and adds to this literature by demonstrating specific cognitive

changes in the CS-US relationship. Note however, that changes in harm expectancies were

not related to treatment outcome in the current study, a finding that contrasts previous work

that established a mediating role of cognitive changes (as assessed by the Posttraumatic

Cognition Inventory; (Foa, Ehlers, Clark, Tolin, & Orsillo, 1999)) on PTSD symptoms during

exposure therapy. Importantly, our findings also contrast the inhibitory learning model, or at

least the clinical implication that exposure sessions should be evaluated by the explicit

evaluation of expectancy violation (as proposed in Craske et al., 2014). Granted that harm

expectancies specifically assess declarative knowledge of the CS-noUS association (“I know I

won’t go crazy”), and extinction learning is thought to rely primarily on lower-level (implicit)

learning, explicit evaluation of harm expectancies might not fully capture corrective learning

during exposure therapy. Tentatively, measures that gauge implicit learning (e.g.

physiological measures) might better reflect extinction processes and be more closely related

to exposure therapy outcome.

9
 Despite the critique on the fear habituation model (Craske, et al., 2008; Craske, et al.,

2014), we found that fear habituation both within and between sessions were moderately

related to PTSD symptom reductions. Surprisingly, we found within session habituation to be

related to treatment outcome, while prior work in PTSD patients failed to find such a

relationship (Nacasch, et al., 2015; van Minnen & Hagenaars, 2002). This finding might be

related to our intensive exposure treatment program, in which patients have several imaginal

exposure sessions per day. Hypothetically, in-session habituation during these back-to-back

sessions is a better proxy of treatment response as compared to in-session responses in weekly

treatment programs.

There are several limitations of our study that deserve mentioning. First, we used a new, theory-

based, PTSD-specific instrument to assess harm expectancies during imaginal exposure therapy.

Although the answers to the open-ended harm expectancies verified our standardized measure, we

cannot rule out that patients would have reported different harm expectancies over the course of

treatment or that personalised expectancy measures would have captured their harm expectancies

better. Up until now, it is still unclear which harm expectancies should exactly be violated during

exposure therapy for PTSD. In Pavlovian fear conditioning the US expectancy refers to the expectancy

of a circumscribed, external threat event (e.g. electric shock), whereas in exposure sessions the harm

expectancy refers most often to the expectancy of subjective, internal threat (e.g. the feeling of losing

control; Soeter & Kindt, 2015). This provides a translational challenge and more work should be done

to further refine harm expectancy measures to be able to examine mechanisms of change during

exposure therapy.

Second, our study protocol allowed for changes in exposure content between therapy sessions,

which may have influenced our indices of between session learning. It would be interesting to learn

the predictive value of expectancy learning for exposure therapy outcome with the same US (i.e.

trauma related stimulus) during all exposure sessions. Third, we only assessed harm expectancies

related to recollecting the traumatic memories, and not related to exposure to other trauma-relevant

10
cues. It would be informative to see whether harm expectancies change during exposure in vivo

assignments, and how this interacts with treatment outcome. Fourth, we assessed outcome at post-

treatment, while a longer follow-up might have provided valuable information. Given that return of

fear (either via spontaneous recovery, renewal or reinstatement) is common after extinction training, it

has been suggested that “extinction is relatively easy to “learn” but difficult to “remember”” (Vervliet,

Craske, & Hermans, 2013, p. 242). As such, the retrievability of the extinction memory (i.e. the US-

noUS association) post-treatment is considered to be pivotal for the long-term efficacy of exposure

therapy (Bouton, 2002; Craske, Liao, Brown, & Vervliet, 2012). Future work should consider

examining the relationship between harm expectancy violation during trauma-focused treatment, its

retention post-treatment and relationship with long-term outcome. Last, the fact that we used DSM-IV

instead of DSM-5 criteria for PTSD should be considered a limitation of the current study.

5. Conclusions

The results from this study highlight the need for valid indices of corrective learning during

exposure therapy for PTSD. Although harm expectancies diminished over the course of

treatment, expectancy violation was not related to treatment outcome, whereas fear

habituation was. The suggestion to use harm expectancy violation instead of fear habituation

measures to monitor patient progress during exposure therapy (Craske, et al., 2014) lacks

empirical support in PTSD. More clinical research is warranted to examine expectancy

violation as a cardinal mechanism of change during imaginal exposure for the treatment of

PTSD.

Acknowledgements: We extend our thanks to all therapists participating in the study. We are also

grateful to everyone, and Cindy Hubers in particular, for helping with the data collection and data

entry.

11
Funding statement: This study was funded by Pro Persona Research; Innovatiefonds

Zorgverzekeraars; and Stichting Achmea Slachtoffer en Samenleving.

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Table 1. Baseline characteristics of study participants.

n (%)

Demographics

Female 44 (88)

Post high school education 37 (74)

Married/Co-habitating 22 (44)

Trauma history

Childhood (≤16 year)

Sexual abuse 43 (86)

Physical abuse 33 (66)

Adult

Sexual assault 25 (50)

Domestic violence/physical assault 27 (54)

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Table 2. Means (SD’s) of expectancy violation and fear habituation measures per imaginal exposure session,

and averaged over treatment (N=50).

Day 1 Day 2 Day 3 Day 4 Mean

Expectancy violation measures

Harm Expectancy 6.45 4.35 3.53 2.85 4.30

(2.43) (3.05) (2.73) (2.78) (2.29)

Harm Experience 3.21 2.61 1.78 1.53 2.28

(2.64) (2.55) (2.20) (2.21) (2.00)

Within session expectancy 3.24 1.74 1.75 1.32 2.02

violation (2.73) (2.95) (2.08) (1.94) (1.81)

Between session expectancy - 2.11 0.82 0.67 1.20

change (2.76) (1.94) (1.80) (0.93)

Fear habituation measures

SUD peak 8.94 9.12 8.70 8.56 8.83

(1.56) (1.21) (1.33) (1.50) (1.15)

SUD end 6.86 6.06 6.20 6.18 6.33

(2.31) (2.95) (2.67) (2.59) (2.33)

Within session habituation 2.08 3.06 2.50 2.38 2.51

(2.13) (2.62) (2.27) (1.86) (1.91)

Between session habituation - -0.18 0.42 0.14 0.13

(1.45) (1.21) (1.07) (0.51)

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Table 3 Correlations between mean expectancy violation and fear habituation measures (N=50).

1. 2. 3. 4.

1. Within session expectancy violation .08 .09 .20

2. Between session expectancy change .39* .32*

3. Within session fear habituation .38*

4. Between session fear habituation

18